Chronic social stress in early life can predispose mice to antisocial maltreating behavior.

Purpose: In our previous study, we developed an assay system to evaluate antisocial maltreating behavior of conspecific mice using a perpetrator-victim paradigm. We also generated a mouse model for the maltreating behavior by mimicking child maltreatment or abuse. Here, we further investigate the antisocial behavior using anti-aggressive and antipsychotic drugs.

Gut microbiome diversity in a febrile seizure mouse model.

Purpose: Febrile seizures at a young age can provoke late-onset temporal lobe epilepsy. Since recent evidence has suggested that the gut microbiome affects central nervous system pathology across the blood-brain barrier, we hypothesized that febrile seizures alter the composition of the gut microbiome to provoke epilepsy.

Methods: Third-generation C57BL/6 mice were separated into two groups (n = 5 each), and hot air was applied to only one group to cause febrile seizures.

Chronic social stress during early development is involved in antisocial maltreatment behavior in mice.

Purpose: Early-life stress can cause brain inflammation and affect social behavior in adulthood. In humans, maltreated (abused or neglected) children often exhibit antisocial behavior, including violent and sadistic behavior, in adulthood. However, it is unknown whether maltreatment behavior occurs in rodents.

Chronic social stress during early development elicits unique behavioral changes in adulthood.

Purpose: Chronic social stress is known to induce inflammation in the brain, and early-life stress affects the brain and social behavior in adulthood. To study the relationship between social stress in childhood development and social behavior in adulthood, we subjected mice to a sequential early-life social stresses and characterized their adult behavioral phenotypes.

Methods: C57BL/6 mice were sequentially subjected to maternal separation (MS), social defeat (SD), and social isolation (SI) in that order.

Proteins related to ictogenesis and seizure clustering in chronic epilepsy.

Seizure clustering is a common phenomenon in epilepsy. Protein expression profiles during a seizure cluster might reflect the pathomechanism underlying ictogenesis. We performed proteomic analyses to identify proteins with a specific temporal expression pattern in cluster phases and to demonstrate their potential pathomechanistic role.

Correction: Clustering of spontaneous recurrent seizures separated by long seizure-free periods: An extended video-EEG monitoring study of a pilocarpine mouse model.

[This corrects the article DOI: 10.1371/journal.pone.

Possible epigenetic regulatory effect of dysregulated circular RNAs in Alzheimer's disease model.

As circular RNAs (circRNAs) regulates the effect of micro RNAs (miRNAs), circRNA-miRNA-mRNA network might be implicated in various disease pathogenesis. Therefore, we evaluated the dysregulated circRNAs in the Tg2576 mouse Alzheimer's disease (AD) model, their possible regulatory effects on downstream target mRNAs, and their pathomechanistic role during the disease progression. The microarray-based circRNA expression analysis at seven- and twelve-months of ages (7 M and 12 M) returned 101 dysregulated circRNAs at 7 M (55 up-regulated and 46 down-regulated) and twelve dysregulated circRNAs at 12 M (five up-regulated and seven down-regulated).

Possible epigenetic regulatory effect of dysregulated circular RNAs in epilepsy.

Circular RNAs (circRNAs) involve in the epigenetic regulation and its major mechanism is the sequestration of the target micro RNAs (miRNAs). We hypothesized that circRNAs might be related with the pathophysiology of chronic epilepsy and evaluated the altered circRNA expressions and their possible regulatory effects on their target miRNAs and mRNAs in a mouse epilepsy model. The circRNA expression profile in the hippocampus of the pilocarpine mice was analyzed and compared with control.

Maternal immune activation alters brain microRNA expression in mouse offspring.

Objective: Maternal immune activation (MIA) is associated with an increased risk of autism spectrum disorder (ASD) in offspring. Herein, we investigate the altered expression of microRNAs (miRNA), and that of their target genes, in the brains of MIA mouse offspring.

Methods: To generate MIA model mice, pregnant mice were injected with polyriboinosinic:polyribocytidylic acid on embryonic day 12.

Trpm2 Ablation Accelerates Protein Aggregation by Impaired ADPR and Autophagic Clearance in the Brain.

TRPM2 a cation channel is also known to work as an enzyme that hydrolyzes highly reactive, neurotoxic ADP-ribose (ADPR). Although ADPR is hydrolyzed by NUT9 pyrophosphatase in major organs, the enzyme is defective in the brain. The present study questions the role of TRPM2 in the catabolism of ADPR in the brain.

Dysregulated long non-coding RNAs in the temporal lobe epilepsy mouse model.

Purpose: To perform comprehensive profiling of long non-coding RNAs (LncRNAs) in temporal lobe epilepsy.

Methods: We performed extensive profiling of LncRNAs and mRNAs in the mouse pilocarpine model in specific brain regions, the hippocampus and cortex, and compared the results to those of the control mouse. Differentially expressed LncRNAs and mRNAs were identified with a microarray analysis (Arraystar Mouse LncRNA Expression Microarray V3.

Clustering of spontaneous recurrent seizures separated by long seizure-free periods: An extended video-EEG monitoring study of a pilocarpine mouse model.

Seizure clustering is a common and significant phenomenon in patients with epilepsy. The clustering of spontaneous recurrent seizures (SRSs) in animal models of epilepsy, including mouse pilocarpine models, has been reported. However, most studies have analyzed seizures for a short duration after the induction of status epilepticus (SE).

Neurovascular Cell Sheet Transplantation in a Canine Model of Intracranial Hemorrhage.

Cell-based therapy for intracerebral hemorrhage (ICH) has a great therapeutic potential. However, methods to effectively induce direct regeneration of the damaged neural tissue after cell transplantation have not been established, which, if done, would improve the efficacy of cell-based therapy. In this study, we aimed to develop a cell sheet with neurovasculogenic potential and evaluate its usefulness in a canine ICH model.

HLA-B*40:02 and DRB1*04:03 are risk factors for oxcarbazepine-induced maculopapular eruption.

Objective: Oxcarbazepine (OXC) is a widely used antiepileptic drug for the treatment of partial seizures that was developed through structural variation of carbamazepine. Although OXC has a lower risk of cutaneous adverse drug reactions (cADRs) than carbamazepine, cADRs ranging from maculopapular eruption (MPE) to the more severe Stevens-Johnson syndrome and toxic epidermal necrolysis still limit the use of OXC in some patients. A few human leukocyte antigen (HLA)-related genetic risk factors for carbamazepine-induced cADRs have been identified.

Protein arginine methylation facilitates KCNQ channel-PIP2 interaction leading to seizure suppression.

KCNQ channels are critical determinants of neuronal excitability, thus emerging as a novel target of anti-epileptic drugs. To date, the mechanisms of KCNQ channel modulation have been mostly characterized to be inhibitory via Gq-coupled receptors, Ca(2+)/CaM, and protein kinase C. Here we demonstrate that methylation of KCNQ by protein arginine methyltransferase 1 (Prmt1) positively regulates KCNQ channel activity, thereby preventing neuronal hyperexcitability.

Distinct intrathecal interleukin-17/interleukin-6 activation in anti-N-methyl-d-aspartate receptor encephalitis.

The aim of this study was to compare serum and cerebrospinal fluid (CSF) cytokine/chemokine levels between anti-NMDAR and anti-LGI1 encephalitis patients. Samples from fourteen anti-NMDAR encephalitis patients, ten anti-LGI1 encephalitis patients, and ten controls were analyzed for the following cytokines/chemokines: IL-1b, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, IL-17A, IL-23, GM-CSF, IFN-gamma, TNF-alpha, and CXCL13. Compared with controls, CSF IL-17A, IL-6 and CXCL13 were elevated in anti-NMDAR encephalitis patients (post-hoc p-values 0.

Altered behavior and neural activity in conspecific cagemates co-housed with mouse models of brain disorders.

The psychosocial environment is one of the major contributors of social stress. Family members or caregivers who consistently communicate with individuals with brain disorders are considered at risk for physical and mental health deterioration, possibly leading to mental disorders. However, the underlying neural mechanisms of this phenomenon remain poorly understood.

Inhibition of miR-203 Reduces Spontaneous Recurrent Seizures in Mice.

Inhibitory synaptic receptors are dysfunctional in epileptic brains, and agents that selectively target these receptors may be effective for the treatment of epilepsy. MicroRNAs interfere with the translation of target genes, including various synaptic proteins. Here, we show that miR-203 regulates glycine receptor-β (Glrb) in epilepsy models.

Prevalence of antineuronal antibodies in patients with encephalopathy of unknown etiology: Data from a nationwide registry in Korea.

We aimed to evaluate the prevalence of antineuronal antibodies in a nationwide cohort of patients with encephalopathy of unknown etiology. We screened 1699 patients with idiopathic encephalopathy who were referred from 70 hospitals across Korea for autoimmune synaptic and classic paraneoplastic antibodies. Those with cerebellar degeneration, sensory polyneuropathy or other paraneoplastic syndromes without encephalopathy were not included in this study.

The complexity of diagnosing postural orthostatic tachycardia syndrome: influence of the diurnal variability.

We investigated how the diagnosis of postural orthostatic tachycardia syndrome (POTS) would be changed due to diurnal variability in orthostatic tachycardia. The orthostatic vital sign test was administered to each patient twice, in the afternoon of the day of admission and the next morning (n = 113). Forty-six patients were diagnosed with POTS, and the remaining 67 patients were assigned to non-POTS group.

Early diagnosis of Alzheimer's disease from elevated olfactory mucosal miR-206 level.

MicroRNA-206, which suppresses the expression of brain-derived neurotrophic factor, is known to be elevated in the brains of Alzheimer's disease (AD) patients. We performed intranasal biopsy of the olfactory epithelia of early dementia patients (n = 24) and cognitively healthy controls (n = 9). Patients with significant depression (n = 8) were analyzed separately, as their cognitive impairments were thought to be caused by their depression.

Effect of Immunotherapy on Seizure Outcome in Patients with Autoimmune Encephalitis: A Prospective Observational Registry Study.

Objective: To evaluate the seizure characteristics and outcome after immunotherapy in adult patients with autoimmune encephalitis (AE) and new-onset seizure.

Methods: Adult (age ≥18 years) patients with AE and new-onset seizure who underwent immunotherapy and were followed-up for at least 6 months were included. Seizure frequency was evaluated at 2-4 weeks and 6 months after the onset of the initial immunotherapy and was categorized as "seizure remission", "> 50% seizure reduction", or "no change" based on the degree of its decrease.

Gamma oscillation in functional brain networks is involved in the spontaneous remission of depressive behavior induced by chronic restraint stress in mice.

Background: Depression is one of the most prevalent mood disorders, and is known to be associated with abnormal functional connectivity in neural networks of the brain. Interestingly, a significant proportion of patients with depression experience spontaneous remission without any treatment. However, the relationship between electroencephalographic (EEG) functional connectivity and the spontaneous remission in depression remains poorly understood.